Activating mutations in IL7R, notably those causing homodimerization of IL-7Rα, such as the S185C substitution in the extracellular domain or insertions or deletions in the transmembrane domain of IL-7R, enhance JAK–STAT5 signaling and are found in approximately 12% of Ph-like ALL and 2–3% of B-ALL cases (180, 181). Here, STAT5A is linked to acute lymphoblastic leukemia.